Delaney T J, Miller E D
Anesthesiology. 1980 Feb;52(2):154-6.
The role of the renin--angiotensin system in the maintenance of blood pressure during halothane anesthesia and sodium nitroprusside (SNP)-induced hypotension was evaluated. Control rats received halothane anesthesia (1 MAC) for one hour, followed by SNP infusion, 40 microgram/kg/min, for 30 min, followed by a 30-min recovery period. A second group of rats was treated identically and, in addition, received an infusion of saralasin (a competitive inhibitor of angiotensin II) throughout the experimental period. In each group, SNP infusion resulted in an initial decrease in blood pressure from 86 torr and 83 torr, respectively, to 48 torr. During the SNP infusion the control animals demonstrated a progressive increase in blood pressure to 61 torr, whereas the saralasin-treated animals showed no change. Following discontinuation of SNP, blood pressure in the control animals rebounded to 94 torr, as compared with 78 torr in the saralasin-treated rats. This study indicates that with stable halothane anesthesia, the partial recovery of blood pressure during SNP infusion and the post-SNP rebound of blood pressure can be completely blocked by saralasin. This demonstrates the participation of the renin--angiotensin system in antagonizing the combined hypotensive effects of halothane and SNP.
评估了肾素 - 血管紧张素系统在氟烷麻醉和硝普钠(SNP)诱导的低血压期间维持血压中的作用。对照大鼠接受氟烷麻醉(1 MAC)1小时,随后以40微克/千克/分钟的速度输注SNP 30分钟,然后有30分钟的恢复期。第二组大鼠接受相同处理,此外,在整个实验期间输注沙拉新(一种血管紧张素II竞争性抑制剂)。在每组中,输注SNP导致血压分别从86托和83托初始降至48托。在输注SNP期间,对照动物的血压逐渐升高至61托,而接受沙拉新治疗的动物则无变化。停止输注SNP后,对照动物的血压反弹至94托,而接受沙拉新治疗的大鼠为78托。本研究表明,在稳定的氟烷麻醉下,输注SNP期间血压的部分恢复以及SNP后血压的反弹可被沙拉新完全阻断。这证明了肾素 - 血管紧张素系统参与拮抗氟烷和SNP的联合降压作用。